Original articlesDetection of Transitory Myocardial Ischemia Secondary to Perinatal Asphyxia
Introduction
Perinatal asphyxia is an important cause of morbimortality and is a frequent cause for admission at neonatal intensive care units (NICU). Since 1862, Little established, for the first time, a close relationship between asphyxia and neurologic lesions.
Perinatal asphyxia is defined as the presence of hypoxia, hypercapnia, and acidosis leading the newborn (NB) to systemic disturbances 1, 2. When an asphyxic event occurs, the organism sets off a series of mechanisms to preserve the necessary mechanisms for all vital organs (brain and heart) to continue working normally, while other organs such as the kidneys, gastrointestinal tract, and skin are affected (target) to a greater or lesser degree based on the duration of the episode 3, 4. When, in spite of compensatory mechanisms, the event prevails, it may affect the heart and brain. In the first case, ischemic hypoxic encephalopathy (IHE) is caused in the full-term and post-term NB, while in the pre-term NB, unspecified changes occur due to the immaturity of the central nervous system. When the heart is affected, transitory myocardial ischemia (TMI), or hypoxic myocardiopathy, as it also is known, may cause an acute myocardial infarction in the most severe case 5, 6, 7, 8.
Few cases have been reported in the literature on TMI. TMI has been described since 1947 through autopsy reports, but it was not until 1972 that Rowe and collaborators described it as transitory heart failure of non-malformative origin and of favorable evolution with symptomatic treatment (9).
The clinical diagnosis of TMI is variable, ranging from tachypnea, congestive heart failure (CHF), tricuspid valve insufficiency murmurs, myocardial infarction to cardiogenic shock 8, 10, although it is most often masked by other concomitant diseases, such as severe ischemic hypoxic encephalopathy per se, respiratory distress syndrome (RDS), massive meconial aspiration syndrome, intracranial hemorrhage, respiratory failure, etc. When ischemia is mild, it may not even be perceptible (11) if not intentionally looked for or may be thought of as a congenital cardiopathy in which a differential diagnosis with other disease must be performed (9).
For its detection, physicians must base their diagnosis not only on clinical data, but also on paraclinical parameters, such as measuring the MB fraction of creatine phosphokinase, electrocardiographic changes pointing to ischemia, lesions or infarctions, chest X-ray showing cardiomegaly (12), and echocardiogram especially for congenital cardiopathy and for appreciating valvular changes when they exist, mainly of the tricuspid valve (13).
In 1983, Jedeikin et al. (14) classified the electrocardiographic changes found in cases of asphyxia after studying healthy and stressed NB. Two years later, the same authors correlated these changes with a rise in CPK-MB, finding that the changes in one do not support TMI. However, when both are abnormal, the majority will suffer TMI (15).
The purpose of the current study is to detect TMI secondary to perinatal asphyxia in a population of asphyxiated NB in comparison with asphyxiated NB with no evidence of TMI.
Section snippets
Materials and Methods
From April 1996 to December 1997, 43 asphyxiated NB were studied. Three were excluded. Patients were divided into two groups: group A patients had TMI and group B patients did not. In group A, there were 33 patients, 15 males and 18 females, and in group B, seven patients, four males and three females. In the first group there were 24 full-term NB and nine pre-term NB; in group B, six full-term and 1 pre-term NB. In neither of the two groups were there post-term NB. The Ballard clinical method
Results
No significant differences were found in gestational ages, birth weights, or extrauterine ages at the time of the study and Apgar scores between the two groups (Table 1). Differences were not found in heart rate on the first day (when admitted to the study) or on the third day, among the groups. However, on the second day, there was a greater increase in heart rates in the group without TMI (group B) (p <0.05) (Table 2).
Similarly, no differences were found in heart rate, electrical axis, nor in
Discussion
The confirmed diagnosis of perinatal asphyxia is difficult to prove clinically because a low Apgar score (6 or lower) should be supported with biochemical criteria 1, 2. However, these tests are not routinely done and some of these methods are not accessible to hospital personnel. Based on the inclusion and exclusion criteria used in this study, the possibility of overdiagnosing asphyxia using Apgar scores is remote.
These cases and controls in a cohort study show the frequency of TMI if
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